Summations Only

Good to talk with you Wounded King Sorry, about my confusion about who cited these articles. Frankly, these articles are an exercise in disrupting preexisting gene sequence to illicit the relative functions involved. What are these citations intended to prove about new unique functionality? Clearly, these alleles preexist in the genome and are not receiving new novel coding sequences (long additional strings of base pair coding) but only experiencing shifts in ORF’s.

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Mutations at both agouti (14, 15) and at Mc1r (16) have been identified that produce unbanded dorsal hairs in the laboratory mouse. We observed banded dorsal hairs in all light C. intermedius, but unbanded, uniformly melanic hairs in all dark C. intermedius, suggesting a possible role for either agouti or Mc1r.
We used association studies with these candidate genes to investigate the genetic basis of adaptive melanism in C. intermedius. Here, we report that mutations at Mc1r are perfectly associated with coat color differences in one population of these mice, but that another population of mice shows no association between Mc1r mutations and coat color phenotype.

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The genetic basis of adaptive melanism in pocket mice - PMC

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What known mutational mechanisms are you referring to would cause an allele arising with only 3 or 4-point mutations? I would say that this is only modification of existing alleles. What would you say this is? How is this argument contrary to the concept of preprogrammed alleles? I would say that there is a lack of understanding of the entire process by the authors. I could easily say that the unknown correlation between specific alleles show a fluidity in the genetic structure. Is this fluidity designed or not that is the underlying question here? Actually DNA ORF’s frame shifting. Yes but the ORF is shifted away from that start codon (the expression is changed). Please explain what is so complicated about this to understand? Maybe I can best express my perspective from a personal viewpoint.I have used random number generators in programs to produce unique program behavior. In other words, my program used the advantage of a random variable to produce useful output. If somehow the random variable was inserted in my core program, the result might crash my efforts (if the exception was not handled properly). Yes the immune system is adaptive in this exact way. Thanks for the exercise in explaining the very processes I am pointing out. If you do not like anticipation, try preemptive or fluid. It is an amazing irreducible system. I am not sure if we can sidetrack on this issue (it has been covered by intelligent design posts). The mechanism is easy to research and is covered by Michael J. Behe. Please provide an example of an observed spontaneous molecular mechanism for the occurrence of a single gene outside the mechanism of duplication. Contrary to the observed evidence, my friend. Drosophila melanogaster is probably the most observed and scrutinized organism in science. For over 80 years scientists have tried all forms of mutagens, cross breeding, inbreeding and there has never been an observed speciation event in DM. The article you cited uses several standard analysis tools geared for inferring common descent and evolution; sorry but this is evaluative speculation at best. The following excerpt from the article lays out my objection:

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However, almost nothing is known about the genes involved in such hybrid incompatibilities or the evolutionary forces that drive their divergence. Here we identify a gene that causes epistatic inviability in hybrids between two fruitfly species, Drosophila melanogaster and D. simulans. Our population genetic analysis reveals that this genewhich encodes a nuclear pore proteinevolved by positive natural selection in both species’ lineages. These results show that a lethal hybrid incompatibility has evolved as a by-product of adaptive protein evolution.

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Here is an article summarizing some of the efforts to cause DM to evolve:

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After decades of study, without immediately killing or sterilizing them, 400 different mutational features have been identified in fruit flies. But none of these changes the fruit fly to a different species.

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2021, 10 Damage to the genome can and does cause reproductive problems but not speciation events. Separated species can be forced to breed and thus show that reproduction in the same species is maintained. Macro changes in genotype are not observed even in separated and reproductive isolated organisms. I would like some examples of yours for my notes. My example is Drosophila melanogaster.I appreciate your knowledge about the subject. Let us reason further on this subject.
Thanks for the citations WK Edited by zaius137, : No reason given.

Chaps, can I suggest that we stick to Taq's mouse paper for a while. It seems to me that we have something there - a novel feature and an observed genetic change that appears causal. So what's wrong with it?Z, let's not get sidetracked into speciation events - that's another topic entirely. and we needn't concern ourselves with a mechanism for the mutation unless we can agree that it has actually occurred. I don't want us to start chasing rabbits again.

That they come about through random mutations, as shown in the paper. The dark phenotype is a novel sequence that was produced by mutations. The mutations changed the ancestral sequence into a sequence that had never existed before in that population. That is the whole point. A novel phenotype came about through mutation, and was then fixed in a population through selective pressures, otherwise known as evolution. Replication errors by polymerases during meiosis, chemical mutagens, radiation, etc.Are you not familiar with how mutations occur? No shit Sherlock. That's how evolution works. Evolution is descent with modification.

This caught my eye in your post because it seemed to me that the modification of existing alleles is exactly what it is and exactly what we're looking for. Why do you shrug it off?

Oh dear, we seem to be running into the creationists not knowing what they are talking about phase of this thread very early. What you seem to be trying to describe has nothing to do with the mutations identified in the melanic Pinacate mouse. I assume that by the rather word salady "DNA ORF’s frame shifting" you are trying to say what they saw was a frame shift mutation, it wasn't. None of the mutations they describe are frame shifts. If you are talking about frame shifts in relation to this paper then you are just making things up. If you aren't talking about frame shifts then I have no idea what it is you are trying to talk about. As others have said, the modification of existing alleles is considered one on the major sources of novel functionality, either in the genes original form or in a duplicated copy. This seems like a remarkably arrogant statement given the tenuous understanding of the paper you have presented so far. Because if there exist preprogrammed alleles, whatever that means, for specific traits then it seems reasonable to expect the same traits in related species to be associated with the same genetic/allelic basis. Given the multiple different genetic bases for melanic phenotypes in mice this seems to suggest that there is no such preprogrammed allele. You could say any nonsense that crossed your mind, why should anyone care? You seem to be using 'fluid' and 'fluidity' to mean that whatever turns out to be the case will be consistent with your hypothesis. Still word salad, words don't mean whatever you want them to mean. A frame shift is when an insertion or deletion of one or more nucleotides disrupts the open reading frame (ORF) of a gene and subsequently changes the reading of the codons downstream of the mutation site. You could consider a mutation which destroyed the start codon to be a form of frame shift, though technically I would dispute that, but either way none of the mutations mentioned in the paper are either of those things, they are neither frame shifts nor disruptions of the start codon. Ah, finally, something to indicate what you actually mean, unfortunately you seem to still be very confused. The ORF is not shifted away from the start codon, for that to happen there would need to be an insertion directly after the start codon. What happened in the black-and-tan mouse is that a distant promoter sequence was disrupted. The one correct element you hit on, there had to be one sometime, is that the effect is associated with a change in regulation. This is an important point because changes in the regulation of expression of genes can be just as important as changes in coding sequence in terms of novel traits. For a good example of this just consider the already mentioned short legged dog phenotype which arose from a duplication of FGF4 leading to a different pattern of expression given the different genetic context the copy was inserted into. Well it is hard for me to understand what you mean because it bears little to no resemblance to how molecular genetics actually works. You seem to have just picked up a whole lot of technical terms without going to the effort of actually understanding what they mean and think that stringing a few together will take the place of a coherent argument. As to why the paper seems so complicated for you to understand, I would be hard put to say, but I think it might be that you just don't have a very good basic understanding of molecular biology and genetics. Dammit Zaius! I gave you the choice of 2 options and your answer is yes? Seriously?!Is it ...A) The mere existence of the immune system anticipates the existence of the phenomenon of infection in general.or ..B) The immune system anticipates specific antigen challenges. I agree, discussing whether the immune system is IC is a topic for another thread, though it is a claim that has already been substantively rebutted. Eh? Do you mean that the excerpt is an example of what you object to? Because it doesn't lay out any objection, it just summarises their finding that they identified a specific molecular basis for hybrid inviability between two species.As to your pathlight reference, this is a frequent and bizarre creationist straw man that almost all drosophila experiments involving mutation have been with the intention to produce a new species, someone should really inform the biologists who were doing the experiments, they will be very surprised.You seem to be, rather unsurprisingly, using the term speciation in an idiosyncratic creationist way that has little to nothing to do with how it is understood in biology. You say that but I get the feeling that you really don't, if you did you might actually take the time to read through the paper thoroughly and understand it, as I suggested, rather than making barely coherent arguments with a whole lot of technical terms just thrown together with a few new terms you seem to have made up.TTFN,WKEdited by Wounded King, : spelling

Hi Tangle, Wounded King, Taq, Zaius, et al, Curiously, I would say that it is a mutation of the existing alleles -- that is how alleles are modified (they don't rearrange themselves eh?).And I would say that the modification spread through the populations because of selection of a trait that was beneficial for the survival of the individuals with the trait.ie -- standard evolution: The question is how do novel features evolve. Here we see a new trait, and we see the creationist pass it off as "adaptation" (eg microevolution) and not different enough ("a dog is still a dog").What will it take?Enjoy.

I was relieved to read this in your paper, Taq: I thought it was just me that was missing something - it turns out that finding direct evidence for mutation leading to new features is tough (but not impossible).I suppose it does mean that finding the audit trail in genes for speciation is orders of magnitude more difficult and may never be seen.

In prokaryotes it is a lot easier due to a genome that is 1/1000th the size of eukaryotes and much simpler regulatory networks. In eukaryotes it can be very difficult to ferret out the mutations that cause a change in morphology. The paper under discussion is a great example of this:

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This difference is controlled in large part by the interaction of two proteins, the melanocortin-1-receptor (MC1R) and the agouti-signaling protein (12—14). MC1R is a G protein-coupled receptor that is highly expressed in melanocytes, the specialized cells that are the site of pigment production. A peptide hormone, -melanocyte-stimulating hormone, typically activates MC1R, resulting in elevated levels of cAMP and increased production of eumelanin. Agouti is an antagonist of MC1R; local expression of agouti results in decreased synthesis of eumelanin and increased production of pheomelanin.

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A change in melanin and pheomelanin can come about through changes in more than one gene. Changes in MC1R or Agouti can change expression patterns. A chaperone protein involved with either of those two genes can once again change expression patterns. A regulatory protein upstream of either gene can change expression patterns. Changes in the expression of the peptide hormone that binds to MC1R can change expression patterns. And this is just for coat color. For morphological features the number of genes involved is an order of magnitude higher.Edited by Taq, : No reason given.

That said, it is still challenging even in prokaryotes. If we look at the ever popular long term evolution experiments in E. coli from Lenski's group we will find a few cases where there is a tie between phenotype and genotype but many more where the linkage is unclear. Even the genetic basis for the much publicised evolution of oxic citrate metabolism is still unclear 4 years later.TTFN,WK

Wounded King my friend Your statement implies that these existing alleles just magically appeared in the first place. They are in the right place at the right time to accept moderate modifications to create novel functionality. I have seen no evidence from you or anyone else demonstrating any new novel phylogenic functions arising in the genome except by genetic recombination. Actually, my statement is derived from the fact these phylogenic characteristics for coloration has escaped the scope of these researchers hypothesis and they jump to the speculative conclusion that:

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indicating that adaptive dark color has evolved independently in this species through changes at different genes.

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Simple balderdash A presumptuous conclusion since they did not specifically identify the genes or process. This particular paper does not make any real findings about multiple alleles in different groups of the same species being responsible for different coat coloration. They just make speculation to explain why there approach failed. Yes, I did read the paper I think your point of novel functionality is better served if there actually were a frame shift by promoter disruption. The alternative is saying damaging genes promotes new and unique functions. Removing components to improve working devices is not uncommon though (but the device is always degraded). I recall a certain self-taught engineer in the 60’s used a similar approach to evolution when engineering electronic devicesConsider the following Earl Madman Muntz

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In the 1940s and 1950s, televisions were very complex pieces of equipment, often containing upwards of 30 vacuum tubes, as well as transformers, rheostats, and other heavy electronics. The consequent high price limited their potential for high volume sales. Muntz determined, through trial and error, that he could remove a significant number of parts and still end up with a monochrome TV that worked very well in urban areas, close to transmission towers. He literally carried a pair of wire clippers around and when he felt that one of his builders was overengineering a circuit, he would begin snipping components out. When the TV stopped functioning, they would reinsert the last part and leave the TV as-is. As a result of removing tubes and greatly simplifying circuits originally designed to boost function in fringe areas (far from transmission towers), Muntz's sets generated less heat; overheating was one of the most common reasons for failure in early sets. The sets also weighed significantly less, because as the circuitry was reduced, smaller in-set power supplies were needed. Additionally, as the power supplies contained expensive copper this further reduced cost.
Madman Muntz - Wikipedia

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Interesting that FGF4 retrogene was found in the wolf; this seems to indicate that the chondrodysplastic phenotype in dogs is just another characteristic that follows Mendelian genetics and it might be correctly said it is a pre-existing characteristic in dogs.

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To further understand the origin of the fgf4 retrogene, we compared haplotypes from the source gene, the retrogene, and the insertion site in both dogs and their wild progenitor, the gray wolf. An Expressed Fgf4 Retrogene Is Associated with Breed-Defining Chondrodysplasia in Domestic Dogs - PMC

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However, since we find a common haplotype of 24Kb surrounding the fgf4 retrogene in 19 short legged breeds it is likely the chondrodysplastic phenotype arose only once, before the division of early dogs into modern breeds. Thereafter, the retrogene and its associated phenotype were both maintained and propagated by breeders for purposes specific to each breed. An Expressed Fgf4 Retrogene Is Associated with Breed-Defining Chondrodysplasia in Domestic Dogs - PMC

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Therefore, what is the point here? You know I am going to claim pre-existing programmed gene sequences and all the evolution nonsense is just that nonsense. How does Ecological genetics actually work on the molecular level maybe I am talking to a future Nobel Prize winner? Please don’t get your panties in a wad the answer is yes by the way. It identified one polymorphic aspect between two separate species, fine. However, conclusions about there common descent is just speculation. This from a related article...

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These results show that a lethal hybrid incompatibility has evolved as a by-product of adaptive protein evolution. Adaptive protein evolution in Drosophila - PubMed

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You are now making presumptuous statements.

If I understand you correctly, what your are saying now is that you DO accept that changes to alleles can lead to novel features.But this isn't good enough because, even though they having demonstrated that the changes to the mice genes resulted in a change of colouration which was then selected for in the wild, it was a result of mixing together genes that already exist in the genome not creating an entirely new gene or set of genes.Is this correct?

No it doesn't, it just accepts the reality that genomes already exist which be modified. This was not always the case but the totally de novo origin of a coding sequence is not relevant in discussing the melanic mouse. Given the fact that we have several instances of such a phenomenon occurring it can hardly be called magical, see New genes in the Human lineage for a discussion of a paper on this in humans. Except they did specifically identify the gene in one case Mc1r and could clearly exclude the causative region that they found in that case as the basis for the other. If you want to argue with their methodology and show it is flawed then you are going to have to actually make an argument rather than just claiming that they have shown nothing.It is true that they didn't characterise the exact molecular mechanism to the extent of identifying the exact responsible mutation or mutations and how it gave rise to the phenotype. I'm at a loss as to how you think this fact takes away what they did show which was the close asociation of the phenotype specifically with these 4 mutations which were not seen in the other population. I never doubted you read it, merely that you understood it. Once again, "a frame shift by promoter disruption" is a biologically meaningless phrase, it describes no known type of mutation. Please stop using these two phrases together. Is it a frame shift or a promoter disruption. If you want to claim it is both then you need to show how such a mutation would satisfy both characterisations, so far you have not done so. And so we come to another common creationist trope, that any change to the system is essentially degradative. The alternative, clearly, is that changing genes promotes new and unique functions. You say damaging without any clear basis in fact. I'm quite happy to admit that there are many case where a beneficial mutation is the result of the total disruption of a gene which is certainly classifiable as degradation, but there are also man instances where this is not the case. Can you explain in what way you consider the mutations described in the pocket mice paper to be degradative? Interesting if were true, sadly you seem to have misunderstood yet another paper. It may well be that this mutation can be found extant in Grey wolves, but there is no evidence for that in this paper. In fact table S4 in the supplementary materials shows that the insertion never occurred in the wolf specimens they studied.What they found was that the 24Kb haplotype for the site into which the retrogene inserted was found in the wolf and further that the FGF4 gene haplotypes in the wolf were similar to those of the retrogene in the short stature dogs. They did not find a retrogene insertion in the wolf. If you still wish to claim they did please provide some evidence. Well the point is that the scientific research clearly shows something and you consistently misinterpret and misrepresent it to try and say it does not.You can claim pre-programming till the cows come home but sou have yet to provide a scintilla of evidence to support that claim. Maybe you are just talking to someone who has studied molecular biology. I was addressing your specific question of why I found your argument so difficult to understand, and explaining that it was because you use terms from molecular genetics but you don't use them in a coherent fashion, the primary example being your persistent use of 'frame shift' to describe things which simply aren't frame shifts. Oh dear, finally we see the inevitable emergence of the underlying creationist troll from beneath its polite veneer. Should I begin assuming that all your other apparent instances of severe reading incomprehension can also be ascribed to this puckish wit? It would make more sense than assuming you are debating in good faith given your apparent inability to correctly understand a single paper that has been discussed. And? What is your point? There is no problem with this in terms of evolutionary theory. The idea that post-mating reproductive isolation occurs as a byproduct of adaptive evolution on a related trait is commonplace. Seriously? You are questioning common descent between 2 different species of Drosophila? You wouldn't even have to go outside of the creationist 'still just fruit flies' comfort zone to accept this one.I guess that Ark must have been pretty crowded with representatives of every biological species concept species on it. Clearly you aren't an adherent of the post-diluvial rapid speciation scenario. I prefer to think of them as astute observations on your pattern of behaviour so far.TTFN,WK

It's hard to know exactly how you're trying to be wrong, because it's not clear what you think the technical terms you're using mean. I know, of course, what they actually mean, but it seems very unlikely that you're using them in that sense. The effect of your posts, then, is pretty much that I sit here wondering: "what in the world can he think adaptation means?" and "what the blue blazes can he mean when he says recombination?" and "did he compose his posts by cutting a genetics textbook into its constituent words and then drawing them at random out of a hat?"Consequently, I end up puzzled. For example, when you write: ... surely when you say "recombination" you can't actually mean recombination, can you? Can you clarify this by telling us what you think the word "recombination" means?

My friend Wounded King You can end your accentus objection; at this point, I am only using the phrase as a foil. And those man instances are? And back via AD Nauseum to that paper that you want to continually use to torment me From citation (15) in that paper Do I see inactivating here? They don’t mean inhibiting existing expression to alter pigmentation do they? But these changes in pigmentation are not really creating new novel traits right. Do really wish to make a straw man out of this? I am amazed on how obtuse someone can get and how it can slow down a conversation. The FGF4 haplotype and insertion site is in the grey wolf. It is one mutation away (a single retrotransposition event). Therefore, you have another example of an existing allele slightly modified to shorten legs of an organism (this also is a degradation of an existing allelic expression).Now you need to get on with the show and demonstrate how unique and novel features arise from any other way but simple modifications to complex alleles and if these modifications are unique and novel. You are correct they did not find the actual retrogene inserted it the wolf but all the necessary genetic code is present. This does not sound unreasonable because if the retrogene appeared in a wild wolf that wolf might not be alive long enough to enjoy benefits of short legs. Unbiased scientific research always bolsters my position. If that were not true, I would not say it. Unfortunately I usually must wade threw evolutionary nonsense and biological machination to get to the point. Does that mean we are no longer friends? I find that every conversation I have it is always beneficial to show some respect to the other individual. I have always found some unexpected opportunity to learn something new from everyone. If they are the same species fine, remember common descent of one species to another is your position not mine. There are different species of fruit flies you know and I do not believe they all came from one ancestor. None of your arguments really seems to want to answer any of the real dilemmas in the new evolution synthesis. Namely:How the modern evolution synthesis can account for

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evolution in terms of changes in gene and genotype frequencies within populations and the processes that convert the variation with populations into more or less permanent variation between species.

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You know the old microevolution, macroevolution thing.
Mostly your examples are reversible when it comes to allele mixing.
Let us get to where and how these new novel innovations or microevolution changes fix in a population
Or is this pushing the thread outside the limits of discussion a convenient escape for the harder questions.Edited by zaius137, : No reason given.

Yes it is. No it isn't. It's a necessary first step.So if you wouldn't mind answering my earlier question we might make faster progress.